Integration of SCADA, GIS, and Call Center Systems for Electrical Power Distribution Management and Planning

In electrical power distribution systems the traditional methods cannot detect the customer fault location in real time and respond to customer complaints at the same time of the outage of the electric power because the required information is scattered among isolated databases. In this paper the combination of Supervisory Control and Data Acquisition (SCADA) and Geographical Information System (GIS) and using SQLCMD against DBSET has been shown to solve this problem better. This paper reducing the response time of the customer waiting when they calling the agent in the call center, creating a model for the integration of real time data in SCADA system against static data in GIS to make online GIS and send data from GIS to CALL CENTER at the same time. The prototype describes the flow of the data between various systems and integrates all in one logical database that contains all data about the customers. The proposed model depends on three major sub-systems: GIS, SCADA, and Call Center systems. The GIS system is base of the model so the change and update in GIS database is available, GIS provides different features like maps, real coordinates and tables. The model contains three different databases, GIS as geo database, SCADA as the real time database and call center as customer information database, all this database will be in one logical global database that contains of spatial information tables, asset information tables, topology information tables, and operation information tables. This method has been shown to significantly improve the accuracy and efficiency of fault detection in distribution networks and to decrease the response time in call centers

Exploring Alternative Octane Specification Methods for Improved Gasoline Knock Resistance in Spark-Ignition Engines

Different octane specification methods were evaluated under rising ethanol blending volumes by adopting a refinery economics model to represent a region in the U.S. It was demonstrated that the traditional octane specification methods, such as the Anti-knock Index (AKI) used in the U.S., or the Research Octane Number (RON) and Motor Octane Number (MON) used in the EU, can lead to counterintuitive drop in octane sensitivity with increased availability of ethanol. This is undesirable for modern gasoline engines that require fuels with high RON and low MON, but it is a consequence of how a refinery reformulates the gasoline blendstock, resulting in more naphtha being used in the final composition. The use of a new specification method based on octane index (OI), with engine constant K = −1, internalizes the diminishing role that MON plays in modern engines, thus ensures that the desirable anti-knock quality is being met either through higher RON and/or higher sensitivity. Initial assessment suggests a potential engine efficiency benefit (~ 1.5%) to be gained simply by switching from an AKI-based specification method to an equivalent OI-based method

Effect of Water Harvesting Techniqueson Soil Properties in the South Omdurman Area- Sudan

Abstract%253A This study was conducted at Khartoum New International Airport, South Omdurman area, Khartoum State, Sudan. A complete randomized block design was followed to study the effect of Holes and Crescents water harvesting techniques on the soil moisture content soil sample were taken prior and immediately after rains and at three weeks intervals. The results indicated that the Holes and Crescents water harvesting techniques affected positively some soil physical properties especially at the upper soil layer (0 ndash%253B 30 cm) which was subjected to excavation by a loader. These soil properties included porosity, field capacity and infiltration rate as they have direct influence on the soil moisture content. The Holes water harvesting techniques showed an increase of 15%25 in soil moisture content resulting in better improvement of the soil physical properties as compared to the Crescents water harvesting techniques, hence the farmer techniques recommended for adoptio

A novel pathogenic mutation of the CYP27B1 gene in a patient with vitamin D-dependent rickets type 1: a case report

BACKGROUND: Rickets can occur due to Vitamin D deficiency or defects in its metabolism. Three rare genetic types of rickets with different alterations of genes have been reported, including: Vitamin D dependent rickets type 1, Vitamin D dependent rickets type 2 or also known as Vitamin D resistant rickets and 25 hydroxylase deficiency rickets. Vitamin D dependent rickets type 1 is inherited in an autosomal recessive pattern, and is caused by mutations in the CYP27B1 gene encoding the 1α-hydroxylase enzyme. We report here a new mutation in CYP27B1, which lead to Vitamin D dependent rickets type 1. CASE PRESENTATION: We report on a 13-month-old Arabic Saudi girl with Vitamin D dependent rickets type 1 presented with multiple fractures and classic features of rickets. A whole exome sequencing identified a novel pathogenic missense mutation (CYP27B1:Homozygous c.1510C > T(p.Q504X)) which results in a protein truncating alteration. Both parents are heterozygous carriers of the mutation. Based on data search in Human Gene Mutation Database, 63 CYP27B1 alterations were reported: only 28.6% are protein truncating (5 nonsense, 13 frameshift insertions/deletions, 0 gross deletions), while 61.9% are non-truncating (38 missense, 1 small in-frame insertions/deletion), and 9.5% are possible protein-truncating (5 splice, 1 regulatory). CONCLUSION: The deleterious effect of this alteration, which was the only mutation detected in the CYP27B1 common gene of Vitamin D dependent rickets type 1 in the proband, and its autosomal recessive inheritance fashion, both support a pathogenic nature of this mutation as the cause of Vitamin D dependent rickets type 1

Do poor patients suffer from inaccurate diagnoses more than well-to-do patients? A randomized control trial

BACKGROUND: Poor patients have greater morbidity and die up to 10 years earlier than patients who have higher socio-economic status. These findings are often attributed to differences in life-style between groups. The present study aimed at investigating the extent to which physicians contribute to the effect by providing relative poorer care, resulting in relative neglect in terms of time spent with a poor patient and more inaccurate diagnoses. METHODS: A randomised experiment with 45 internal medicine residents. Doctors diagnosed 12 written clinical vignettes that were exactly the same except for the description of the patients' socio-economic status. Each participant diagnosed four of the vignettes in a poor-patient version, fou

Comprehensive Screening of Eight Known Causative Genes in Congenital Hypothyroidism With Gland-in-Situ.

CONTEXT: Lower TSH screening cutoffs have doubled the ascertainment of congenital hypothyroidism (CH), particularly cases with a eutopically located gland-in-situ (GIS). Although mutations in known dyshormonogenesis genes or TSHR underlie some cases of CH with GIS, systematic screening of these eight genes has not previously been undertaken. OBJECTIVE: Our objective was to evaluate the contribution and molecular spectrum of mutations in eight known causative genes (TG, TPO, DUOX2, DUOXA2, SLC5A5, SLC26A4, IYD, and TSHR) in CH cases with GIS. Patients, Design, and Setting: We screened 49 CH cases with GIS from 34 ethnically diverse families, using next-generation sequencing. Pathogenicity of novel mutations was assessed in silico. PATIENTS, DESIGN, AND SETTING: We screened 49 CH cases with GIS from 34 ethnically diverse families, using next-generation sequencing. Pathogenicity of novel mutations was assessed in silico. RESULTS: Twenty-nine cases harbored likely disease-causing mutations. Monogenic defects (19 cases) most commonly involved TG (12), TPO (four), DUOX2 (two), and TSHR (one). Ten cases harbored triallelic (digenic) mutations: TG and TPO (one); SLC26A4 and TPO (three), and DUOX2 and TG (six cases). Novel variants overall included 15 TG, six TPO, and three DUOX2 mutations. Genetic basis was not ascertained in 20 patients, including 14 familial cases. CONCLUSIONS: The etiology of CH with GIS remains elusive, with only 59% attributable to mutations in TSHR or known dyshormonogenesis-associated genes in a cohort enriched for familial cases. Biallelic TG or TPO mutations most commonly underlie severe CH. Triallelic defects are frequent, mandating future segregation studies in larger kindreds to assess their contribution to variable phenotype. A high proportion (∼41%) of unsolved or ambiguous cases suggests novel genetic etiologies that remain to be elucidated.This study made use of data generated by the UK10K Project and we acknowledge the contribution of the UK10K Consortium. This work was supported by Wellcome Trust Grants 100585/Z/12/Z (to N.S.), and 095564/Z/11/Z (to V.K.C.) and the National Institute for Health Research Cambridge Biomedical Research Center (to V.K.C., N.S.). E.G.S and C.A.A. are supported by the Wellcome Trust (098051). Funding for the UK10K Project was provided by the Wellcome Trust under award WT091310

Population Genomics Related to Adaptation in Elite Oat Germplasm

Six hundred thirty five oat ( L.) lines and 4561 single-nucleotide polymorphism (SNP) loci were used to evaluate population structure, linkage disequilibrium (LD), and genotype–phenotype association with heading date. The first five principal components (PCs) accounted for 25.3% of genetic variation. Neither the eigenvalues of the first 25 PCs nor the cross-validation errors from = 1 to 20 model-based analyses suggested a structured population. However, the PC and = 2 model-based analyses supported clustering of lines on spring oat vs. southern United States origin, accounting for 16% of genetic variation ( < 0.0001). Single-locus -statistic () in the highest 1% of the distribution suggested linkage groups that may be differentiated between the two population subgroups. Population structure and kinship-corrected LD of = 0.10 was observed at an average pairwise distance of 0.44 cM (0.71 and 2.64 cM within spring and southern oat, respectively). On most linkage groups LD decay was slower within southern lines than within the spring lines. A notable exception was found on linkage group Mrg28, where LD decay was substantially slower in the spring subpopulation. It is speculated that this may be caused by a heterogeneous translocation event on this chromosome. Association with heading date was most consistent across location-years on linkage groups Mrg02, Mrg12, Mrg13, and Mrg24

Molecular markers of anti-malarial drug resistance in Lahj Governorate, Yemen: baseline data and implications

<p>Abstract</p> <p>Background</p> <p>This is an investigation of anti-malarial molecular markers coupled with a therapeutic efficacy test of chloroquine (CQ) against falciparum malaria in an area of unstable malaria in Lahj Governorate, Yemen. The study was aimed at assessment of therapeutic response to CQ and elucidation of baseline information on molecular markers for <it>Plasmodium falciparum </it>resistance against CQ and sulphadoxine/pyrimethamine (SP).</p> <p>Methods</p> <p>Between 2002 and 2003 the field test was conducted according to the standard WHO protocol to evaluate the therapeutic efficacy of CQ in 124 patients with falciparum malaria in an endemic area in Lahj Governorate in Yemen. Blood samples collected during this study were analysed for <it>P. falciparum </it>chloroquine resistance transporter gene (<it>pfcrt</it>)-76 polymorphisms, mutation <it>pfcrt-</it>S163R and the antifolate resistance-associated mutations dihydrofolate reductase (<it>dhfr</it>)-C59R and dihydropteroate synthase (<it>dhps</it>)-K540E. Direct DNA sequencing of the <it>pfcrt </it>gene from three representative field samples was carried out after DNA amplification of the 13 exons of the <it>pfcrt </it>gene.</p> <p>Results</p> <p>Treatment failure was detected in 61% of the 122 cases that completed the 14-day follow-up. The prevalence of mutant <it>pfcrt </it>T76 was 98% in 112 amplified pre-treatment samples. The presence of <it>pfcrt </it>T76 was poorly predictive of <it>in vivo </it>CQ resistance (PPV = 61.8%, 95% CI = 52.7-70.9). The prevalence of <it>dhfr </it>Arg-59 mutation in 99 amplified samples was 5%, while the <it>dhps </it>Glu-540 was not detected in any of 119 amplified samples. Sequencing the <it>pfcrt </it>gene confirmed that Yemeni CQ resistant <it>P. falciparum </it>carry the old world (Asian and African) CQ resistant haplotype CVIETSESI at positions 72,73,74,75,76,220,271, 326 and 371.</p> <p>Conclusion</p> <p>This is the first study to report baseline information on the characteristics and implications of anti-malarial drug resistance markers in Yemen. It is also the first report of the haplotype associated with CQR <it>P. falciparum </it>parasites from Yemen. Mutant <it>pfcrt</it>T76 is highly prevalent but it is a poor predictor of treatment failure in the study population. The prevalence of mutation <it>dhfr</it>Arg59 is suggestive of emerging resistance to SP, which is currently a component of the recommended combination treatment of falciparum malaria in Yemen. More studies on these markers are recommended for surveillance of resistance in the study area.</p